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Hemoglobin subunit beta interacts with the capsid protein and antagonizes the growth of classical swine fever virus

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Hemoglobin subunit beta interacts with the capsid protein and antagonizes the growth of classical swine fever virus. / Li, Dan; Dong, Hong; Li, Su et al.

In: Journal of Virology, Vol. 87, No. 10, 05.2013, p. 5707-5717.

Research output: Contribution to Journal/MagazineJournal articlepeer-review

Harvard

Li, D, Dong, H, Li, S, Munir, M, Chen, J, Luo, Y, Sun, Y, Liu, L & Qiu, H-J 2013, 'Hemoglobin subunit beta interacts with the capsid protein and antagonizes the growth of classical swine fever virus', Journal of Virology, vol. 87, no. 10, pp. 5707-5717. https://doi.org/10.1128/JVI.03130-12

APA

Li, D., Dong, H., Li, S., Munir, M., Chen, J., Luo, Y., Sun, Y., Liu, L., & Qiu, H-J. (2013). Hemoglobin subunit beta interacts with the capsid protein and antagonizes the growth of classical swine fever virus. Journal of Virology, 87(10), 5707-5717. https://doi.org/10.1128/JVI.03130-12

Vancouver

Li D, Dong H, Li S, Munir M, Chen J, Luo Y et al. Hemoglobin subunit beta interacts with the capsid protein and antagonizes the growth of classical swine fever virus. Journal of Virology. 2013 May;87(10):5707-5717. Epub 2013 Mar 13. doi: 10.1128/JVI.03130-12

Author

Li, Dan ; Dong, Hong ; Li, Su et al. / Hemoglobin subunit beta interacts with the capsid protein and antagonizes the growth of classical swine fever virus. In: Journal of Virology. 2013 ; Vol. 87, No. 10. pp. 5707-5717.

Bibtex

@article{0fb3a923010a466b906878c4d4284b07,
title = "Hemoglobin subunit beta interacts with the capsid protein and antagonizes the growth of classical swine fever virus",
abstract = "The capsid (C) protein of the Flaviviridae family members is involved in nucleocapsid formation and virion assembly. However, the influence of C protein-interacting partners on the outcome of pestivirus infections is poorly defined. In this study, hemoglobin subunit beta (HB) was identified as a C protein-binding protein by glutathione S-transferase pulldown and subsequent mass spectrometry analysis of PK-15 cells, which are permissive cells for classical swine fever virus (CSFV). Coimmunoprecipitation and confocal microscopy confirmed that HB interacts and colocalizes with the C protein in the cytoplasm. Silencing of HB with small interfering RNAs promoted CSFV growth and replication, whereas overexpression of HB suppressed CSFV replication and growth. Interestingly, HB was found to interact with retinoic acid-inducible gene I and increase its expression, resulting in increased production of type I interferon (IFN). However, HB was unable to suppress CSFV growth when the RIG-I pathway was blocked. Overall, our results suggest that cellular HB antagonizes CSFV growth and replication by triggering IFN signaling, and might represent a novel antiviral restriction factor. This study reports for the first time the novel role of HB in innate immunity.",
keywords = "Animals, Capsid Proteins, Cell Line, Centrifugation, Classical swine fever virus, Flaviviridae, Hemoglobins, Host-Pathogen Interactions, Humans, Immunoprecipitation, Mass Spectrometry, Microscopy, Confocal, Pestivirus, Protein Binding, Protein Interaction Mapping, Protein Subunits, Swine, Virus Assembly, Virus Replication, Journal Article, Research Support, Non-U.S. Gov't",
author = "Dan Li and Hong Dong and Su Li and Muhammad Munir and Jianing Chen and Yuzi Luo and Yuan Sun and Lihong Liu and Hua-Ji Qiu",
year = "2013",
month = may,
doi = "10.1128/JVI.03130-12",
language = "English",
volume = "87",
pages = "5707--5717",
journal = "Journal of Virology",
issn = "0022-538X",
publisher = "American Society for Microbiology",
number = "10",

}

RIS

TY - JOUR

T1 - Hemoglobin subunit beta interacts with the capsid protein and antagonizes the growth of classical swine fever virus

AU - Li, Dan

AU - Dong, Hong

AU - Li, Su

AU - Munir, Muhammad

AU - Chen, Jianing

AU - Luo, Yuzi

AU - Sun, Yuan

AU - Liu, Lihong

AU - Qiu, Hua-Ji

PY - 2013/5

Y1 - 2013/5

N2 - The capsid (C) protein of the Flaviviridae family members is involved in nucleocapsid formation and virion assembly. However, the influence of C protein-interacting partners on the outcome of pestivirus infections is poorly defined. In this study, hemoglobin subunit beta (HB) was identified as a C protein-binding protein by glutathione S-transferase pulldown and subsequent mass spectrometry analysis of PK-15 cells, which are permissive cells for classical swine fever virus (CSFV). Coimmunoprecipitation and confocal microscopy confirmed that HB interacts and colocalizes with the C protein in the cytoplasm. Silencing of HB with small interfering RNAs promoted CSFV growth and replication, whereas overexpression of HB suppressed CSFV replication and growth. Interestingly, HB was found to interact with retinoic acid-inducible gene I and increase its expression, resulting in increased production of type I interferon (IFN). However, HB was unable to suppress CSFV growth when the RIG-I pathway was blocked. Overall, our results suggest that cellular HB antagonizes CSFV growth and replication by triggering IFN signaling, and might represent a novel antiviral restriction factor. This study reports for the first time the novel role of HB in innate immunity.

AB - The capsid (C) protein of the Flaviviridae family members is involved in nucleocapsid formation and virion assembly. However, the influence of C protein-interacting partners on the outcome of pestivirus infections is poorly defined. In this study, hemoglobin subunit beta (HB) was identified as a C protein-binding protein by glutathione S-transferase pulldown and subsequent mass spectrometry analysis of PK-15 cells, which are permissive cells for classical swine fever virus (CSFV). Coimmunoprecipitation and confocal microscopy confirmed that HB interacts and colocalizes with the C protein in the cytoplasm. Silencing of HB with small interfering RNAs promoted CSFV growth and replication, whereas overexpression of HB suppressed CSFV replication and growth. Interestingly, HB was found to interact with retinoic acid-inducible gene I and increase its expression, resulting in increased production of type I interferon (IFN). However, HB was unable to suppress CSFV growth when the RIG-I pathway was blocked. Overall, our results suggest that cellular HB antagonizes CSFV growth and replication by triggering IFN signaling, and might represent a novel antiviral restriction factor. This study reports for the first time the novel role of HB in innate immunity.

KW - Animals

KW - Capsid Proteins

KW - Cell Line

KW - Centrifugation

KW - Classical swine fever virus

KW - Flaviviridae

KW - Hemoglobins

KW - Host-Pathogen Interactions

KW - Humans

KW - Immunoprecipitation

KW - Mass Spectrometry

KW - Microscopy, Confocal

KW - Pestivirus

KW - Protein Binding

KW - Protein Interaction Mapping

KW - Protein Subunits

KW - Swine

KW - Virus Assembly

KW - Virus Replication

KW - Journal Article

KW - Research Support, Non-U.S. Gov't

U2 - 10.1128/JVI.03130-12

DO - 10.1128/JVI.03130-12

M3 - Journal article

C2 - 23487454

VL - 87

SP - 5707

EP - 5717

JO - Journal of Virology

JF - Journal of Virology

SN - 0022-538X

IS - 10

ER -